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Updated: Jan 31, 2026

Author Spotlight: Investigating HR-Dependent Cardiac Function in Mouse Models Through a Novel Atrial-Pacing Approach
Published on: July 21, 2023
miRNA-130a improves cardiac function by down-regulating TNF-α expression in a rat model of heart failure
1Department of Cardiovascular Medicine, The First College of Clinical Medical Science, Three Gorges University, China; Yichang Central People's Hospital, Yichang City, Hubei Province, China. yangxu5946@163.com.
Objective:
To investigate the effect of MicroRNA (miRNA)-130a on cardiac function and the expression of tumor necrosis factor-α (TNF-α) in rats with heart failure.
Materials And Methods:
The rat heart failure model (n = 30) were established, then divided into miRNA-130a group, phosphate-buffer saline (PBS) group, rAAV9 group, and sham group (n = 10 in each group). Four weeks after the operation, the cardiac ultrasound and hemodynamic determination were performed. Blood endothelin-1 (ET-1) content was measured by enzyme-linked immunosorbent assay (ELISA). Hematoxylin and eosin (HE) staining was used to observe the morphology of myocardium. The expression levels of miRNA-130a and TNF-α were determined by quantitative Real Time-Polymerase Chain Reaction) (qRT-PCR). And the expression of TNF-α protein was determined by immunohistochemistry and Western blotting.
Results:
The rat heart failure model was successfully constructed. The miRNA-130a expression was decreased in rats with heart failure, and miRNA-130a transfection was successful. miRNA-130a improved left ventricular ejection fraction in the rat with heart failure. The blood ET-1 in miRNA-130a group was significantly lower than that of PBS group and rAAV9 group (p < 0.05). RT-PCR, Immunohistochemistry and Western blotting results showed that compared with the sham group, the expression of TNF-α in the model group was increased. And the expression of TNF-α in miRNA-130a group was significantly lower than that of PBS and rAAV9 group.
Conclusions:
miRNA-130a could improve cardiac function of heart failure rat by down-regulating TNF-α.
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